A wide variety of implantable medical devices for delivering a therapy or monitoring a physiologic condition have been clinically implanted or proposed for clinical implantation in patients. Some implantable medical devices may employ one or more elongated electrical leads and/or sensors. In some cases, implantable medical devices deliver electrical stimulation therapy and/or monitor physiological signals via one or more electrodes or sensor elements, which may be included as part of one or more elongated implantable medical leads. Implantable medical leads may be configured to allow electrodes or sensors to be positioned at desired locations for delivery of stimulation or sensing. For example, electrodes or sensors may be located at a distal portion of the lead. A proximal portion of the lead may be coupled to an implantable medical device housing, which may contain electronic circuitry such as stimulation generation and/or sensing circuitry.
Implantable medical devices can be configured to deliver cardiac therapy such as cardiac resynchronization therapy (CRT) to treat patients suffering from congestive heart failure. CRT involves either delivering pacing stimulus to both ventricles or to one ventricle with the desired result of a more or less simultaneous mechanical contraction and ejection of blood from the ventricles. Delivering pacing stimulus to both ventricles is referred to as biventricular pacing (BV) while monoventricular pacing refers to left ventricular (LV) pacing, or right ventricular (RV) only pacing, often with fusion from intrinsic conduction if there is intact atrio-ventricular conduction.
CRT improves heart chamber synchrony. Improved heart chamber synchrony may enhance hemodynamic performance of the heart thereby alleviating symptoms of congestive heart failure. Exemplary hemodynamic parameters include ventricular pressure and/or the rate of change in ventricular pressure. Achieving a positive clinical benefit from CRT is dependent on several therapy control parameters, such as the atrio-ventricular (AV) delay and the inter-ventricular (VV) delay. The AV delay controls the timing of ventricular pacing pulses relative to an atrial depolarization, intrinsic or paced. The VV delay controls the timing of a pacing pulse in one ventricle relative to a paced or intrinsic sensed event in the other ventricle.
Selecting optimal AV and VV delays for use in controlling CRT pacing pulses may be affected by local tissue latency. Local tissue latency involves the substantially delayed response time to pace stimulation that occurs at the pace/sense lead electrode to tissue interface. Local tissue latency may be caused by diseased substrate (e.g. scar, fibrosis, etc.) or local conduction block around the site of the pacing electrode. Local tissue latency may have important implications for CRT pacing therapies. For example, if there is latency in a LV lead, it may result in simultaneous BV pacing thereby appearing as RV only pacing which is not as beneficial for the patient. A need remains, therefore, for a device and method that detects local tissue latency and, in response, adjusts one or more CRT pacing control parameters.